The core insight of the resilience-stability tradeoff is that stability leads to loss of resilience. Therefore stabilisation too leads to increased systemic fragility. But there is a lot more to it. In comparing economic crises to forest fires and river floods, I have highlighted the common patterns to the process of system fragilisation which eventually leaves the system “manager” in a situation where there are no good options left.
Drawing upon the work of Mancur Olson, I have explored how the buildup of special interests means that stability is self-reinforcing. Once rent-seeking has achieved sufficient scale, “distributional coalitions have the incentive and..the power to prevent changes that would deprive them of their enlarged share of the social output”. But what if we “solve” the Olsonian problem? Would that mitigate the problem of increased stabilisation and fragility? In this post, I will argue that the cycle of fragility and collapse has much deeper roots than any particular form of democracy.
In this analysis, I am going to move away from ecological analogies and instead turn to an example from modern medicine. In particular, I am going to compare the experience and history of psychiatric medication in the second half of the twentieth century to some of the issues we have already looked at in macroeconomic and ecological stabilisation. I hope to convince you that the uncanny similarities in the patterns observed in stabilised systems across such diverse domains are not a coincidence. In fact, the human body provides us with a much closer parallel to economic systems than even ecological systems with respect to the final stages of stabilisation. Most ecological systems collapse sooner simply because the limits to which resources will be spent in an escalating fashion to preserve stability are much smaller. For example, there are limits to the resources that will be deployed to prevent a forest fire, no matter how catastrophic. On the other hand, the resources that will be deployed to prevent collapse of any system that is integral to human beings are much larger.
Even by the standards of this blog, this will be a controversial article. In my discussion of psychiatric medicine I am relying primarily on Robert Whitaker’s excellent but controversial and much-disputed book ‘Anatomy of an Epidemic’. Nevertheless, I want to emphasise that my ultimate conclusions are much less incendiary than those of Whitaker. In the same way that I want to move beyond an explanation of the economic crisis that relies on evil bankers, crony capitalists and self-interested technocrats, I am trying to move beyond an explanation that blames evil pharma and misguided doctors for the crisis in mental health. I am not trying to imply that fraud and rent-seeking does not have a role to play. I am arguing that even if we eliminate them, the aim of a resilient economic and social system would not be realised.
The puzzle of the history of macroeconomic stabilisation post-WW2 can be summarised as follows. Clearly every separate event of macroeconomic stabilisation works. Most monetary and fiscal interventions result in a rise in the financial markets, NGDP expectations and economic performance in the short run. Yet,
- we are in the middle of a ‘great stagnation’ and have been for a few decades.
- the frequency of crises seems to have risen dramatically in the last fifty years culminating in the environment since 2008 which is best described as a perpetual crisis.
- each recovery seems to be weaker than the previous one and requires an increased injection of stimulus to achieve results that were easily achieved by a simple rate cut not that long ago.
Similarly, the history of mental health post-WW2 too has been a puzzle and is summarised by Whitaker as follows:
The puzzle can now be precisely summed up. On the one hand, we know that many people are helped by psychiatric medications. We know that many people stabilize well on them and will personally attest to how the drugs have helped them lead normal lives. Furthermore, as Satcher noted in his 1999 report, the scientific literature does document that psychiatric medications, at least over the short term, are “effective.” Psychiatrists and other physicians who prescribe the drugs will attest to that fact, and many parents of children taking psychiatric drugs will swear by the drugs as well. All of that makes for a powerful consensus: Psychiatric drugs work and help people lead relatively normal lives. And yet, at the same time, we are stuck with these disturbing facts: The number of disabled mentally ill has risen dramatically since 1955, and during the past two decades, a period when the prescribing of psychiatric medications has exploded, the number of adults and children disabled by mental illness has risen at a mind-boggling rate.
Whitaker then asks the obvious but heretical question – “Could our drug-based paradigm of care, in some unforeseen way, be fueling this modern-day plague?” and answers the question in the affirmative. But what are the precise mechanisms and patterns that underlie this deterioration?
Adaptive Response to Intervention and Drug Dependence
The fundamental reason why interventions fail in complex adaptive systems is the adaptive response triggered by the intervention that subverts the aim of the intervention. Moreover once the system is artificially stabilised and system agents have adapted to this new stability, the system cannot cope with any abrupt withdrawal of the stabilising force. For example, Whitaker notes that
Neuroleptics put a brake on dopamine transmission, and in response the brain puts down the dopamine accelerator (the extra D2 receptors). f the drug is abruptly withdrawn, the brake on dopamine is suddenly released while the accelerator is still pressed to the floor. The system is now wildly out of balance, and just as a car might careen out of control, so too the dopaminergic pathways in the brain……In short, initial exposure to neuroleptics put patients onto a path where they would likely need the drugs for life.
benzodiazepines….work by perturbing a neurotransmitter system, and in response, the brain undergoes compensatory adaptations, and as a result of this change, the person becomes vulnerable to relapse upon drug withdrawal. That difficulty in turn may lead some to take the drugs indefinitely.
(antidepressants) perturb neurotransmitter systems in the brain. This leads to compensatory processes that oppose the initial acute effects of a drug…. When drug treatment ends, these processes may operate unopposed, resulting in appearance of withdrawal symptoms and increased vulnerability to relapse.
Similarly, when a central bank protects incumbent banks against liquidity risk, the banks choose to hold progressively more illiquid portfolios. When central banks provide incumbent banks with cheap funding in times of crisis to prevent failure and creditor losses, the banks choose to take on more leverage. This is similar to what John Adams has termed the ‘risk thermostat’ – the system readjusts to get back to its preferred risk profile. The protection once provided is almost impossible to withdraw without causing systemic havoc as agents adapt to the new stabilised reality and lose the ability to survive in an unstabilised environment.
Of course, in economic systems when agents actively intend to arbitrage such commitments by central banks, it is simply a form of moral hazard. But such an adaptation can easily occur via the natural selective forces at work in an economy – those who fail to take advantage of the Greenspan/Bernanke put simply go bust or get fired. In our brain the adaptation simply reflects homeostatic mechanisms selected for by the process of evolution.
Transformation into a Pathological State, Loss of Core Functionality and Deterioration of the Baseline State
I have argued in many posts that the successive cycles of Minskyian stabilisation have a role to play in the deterioration in the structural performance of the real economy which has manifested itself as ‘The Great Stagnation’. The same conclusion holds for many other complex adaptive systems and our brain is no different. Stabilisation kills much of what makes human beings creative. Innovation and creativity are fundamentally disequilibrium processes so it is no surprise that an environment of stability does not foster them. Whitaker interviews a patient on antidepressants who said: “I didn’t have mood swings after that, but instead of having a baseline of functioning normally, I was depressed. I was in a state of depression the entire time I was on the medication.”
when researchers looked at whether Ritalin at least helped hyperactive children fare well academically, to get good grades and thus succeed as students, they found that it wasn’t so. Being able to focus intently on a math test, it turned out, didn’t translate into long-term academic achievement. This drug, Sroufe explained in 1973, enhances performance on “repetitive, routinized tasks that require sustained attention,” but “reasoning, problem solving and learning do not seem to be [positively] affected.”……Carol Whalen, a psychologist from the University of California at Irvine, noted in 1997 that “especially worrisome has been the suggestion that the unsalutary effects [of Ritalin] occur in the realm of complex, high-order cognitive functions such as flexible problem-solving or divergent thinking.”
Progressive Increase in Required Dosage
In economic systems, this steady structural deterioration means that increasing amounts of stimulus need to be applied in successive cycles of stabilisation to achieve the same levels of growth. Whitaker too identifies a similar tendency:
Over time, Chouinard and Jones noted, the dopaminergic pathways tended to become permanently dysfunctional. They became irreversibly stuck in a hyperactive state, and soon the patient’s tongue was slipping rhythmically in and out of his mouth (tardive dyskinesia) and psychotic symptoms were worsening (tardive psychosis). Doctors would then need to prescribe higher doses of antipsychotics to tamp down those tardive symptoms.
At this point, some of you may raise the following objection: so what if the new state is pathological? Maybe capitalism with its inherent instability is itself pathological. And once the safety nets of the Greenspan/Bernanke put, lender-of-last-resort programs and too-big-to-fail bailouts are put in place why would we need or want to remove them? If we simply medicate the economy ad infinitum, can we not avoid collapse ad infinitum?
This argument however is flawed.
- The ability of economic players to reorganise to maximise the rents extracted from central banking and state commitments far exceeds the the resources available to the state and the central bank. The key reason for this is the purely financial nature of this commitment. For example, if the state decided to print money and support the price of corn at twice its natural market price, then it could conceivably do so forever. Sooner or later, rent extractors will run up against natural resource limits – for example,limits on arable land. But when the state commits to support a credit money dominant financial system and asset prices then the economic system can and will generate financial “assets” without limit to take advantage of this commitment. The only defense that the CB and the state possess is regulations aimed at maintaining financial markets in an incomplete, underdeveloped state where economic agents do not possess the tools to game the system. Unfortunately as Minsky and many others have documented, the pace of financial innovation over the last half-century has meant that banks and financialised corporates have all the tools they need to circumvent regulations and maximise rent extraction.
- Even in a modern state that can print its own fiat currency, the ability to maintain financial commitments is subordinate to the need to control inflation. But doesn’t the complete absence of inflationary pressures in the current environment prove that we are nowhere close to any such limits? Not quite – As I have argued before, the current macroeconomic policy is defined by an abandonment of the full employment target in order to mitigate any risk of inflation whatsoever. The inflationary risk caused by rent extraction from the stabilisation commitment is being counterbalanced by a “reserve army of labour”. The reason for giving up the full employment is simple – As Minsky identified, once the economy has gone through successive cycles of stabilisation, it is prone to ‘rapid cycling’.
Rapid Cycling and Transformation of an Episodic Illness into a Chronic Illness
Minsky noted that
A high-investment, high-profit strategy for full employment – even with the underpinning of an active fiscal policy and an aware Federal Reserve system – leads to an increasingly unstable financial system, and an increasingly unstable economic performance. Within a short span of time, the policy problem cycles among preventing a deep depression, getting a stagnant economy moving again, reining in an inflation, and offsetting a credit squeeze or crunch.
In other words, an economy that attempts to achieve full employment will yo-yo uncontrollably between a state of debt-deflation and high, variable inflation – somewhat similar to a broken shower that only runs either too hot or too cold. The abandonment of the full employment target enables the system to postpone this point of rapid cycling.
The structural malformation of the economic system due to the application of increasing levels of stimulus to the task of stabilisation means that the economy has lost the ability to generate the endogenous growth and innovation that it could before it was so actively stabilised. The system has now been homogenised and is entirely dependent upon constant stimulus. The phenomenon of ‘rapid cycling’ explains a phenomenon I noted in an earlier post which is the apparently schizophrenic nature of the markets, turning from risk-on to risk-off at the drop of a hat. It is the lack of diversity that causes this as the vast majority of agents change their behaviour based on absence or presence of stabilising interventions.
Whitaker again notes the connection between medication and rapid cycling in many instances:
As early as 1965, before lithium had made its triumphant entry into American psychiatry, German psychiatrists were puzzling over the change they were seeing in their manic-depressive patients. Patients treated with antidepressants were relapsing frequently, the drugs “transforming the illness from an episodic course with free intervals to a chronic course with continuous illness,” they wrote. The German physicians also noted that in some patients, “the drugs produced a destabilization in which, for the first time, hypomania was followed by continual cycling between hypomania and depression.””
(stimulants) cause children to cycle through arousal and dysphoric states on a daily basis. When a child takes the drug, dopamine levels in the synapse increase, and this produces an aroused state. The child may show increased energy, an intensified focus, and hyperalertness. The child may become anxious, irritable, aggressive, hostile, and unable to sleep. More extreme arousal symptoms include obsessive-compulsive and hypomanic behaviors. But when the drug exits the brain, dopamine levels in the synapse sharply drop, and this may lead to such dysphoric symptoms as fatigue, lethargy, apathy, social withdrawal, and depression. Parents regularly talk of this daily “crash.”
THE PATIENT WANTS STABILITY TOO
At this point, I seem to be arguing that stabilisation is all just a con-game designed to enrich evil bankers, evil pharma etc. But such an explanation underestimates just how deep-seated the temptation and need to stabilise really is. The most critical component that it misses out on is the fact that the “patient” in complex adaptive systems is as eager to choose stability over resilience as the doctor is.
The Short-Term vs The Long-Term
As Daniel Carlat notes, the reality is that on the whole, psychiatric drugs “work” at least in the short term. Similarly, each individual act of macroeconomic stabilisation such as a lender-of-last-resort intervention, quantitative easing or a rate cut clearly has a positive impact on the short-term performance of both asset markets and the economy.
Whitaker too acknowledges this:
Those are the dueling visions of the psychopharmacology era. If you think of the drugs as “anti-disease” agents and focus on short-term outcomes, the young lady springs into sight. If you think of the drugs as “chemical imbalancers” and focus on long-term outcomes, the old hag appears. You can see either image, depending on where you direct your gaze.
The critical point here is that just like in forest fires and macroeconomies, the initial attempts to stabilise can be achieved easily and with very little medication. The results may seem even miraculous. But this initial period does not last. From one of many cases Whitaker quotes:
at first, “it was like a miracle,” she says. Andrew’s fears abated, he learned to tie his shoes, and his teachers praised his improved behavior. But after a few months, the drug no longer seemed to work so well, and whenever its effects wore off, there would be this “rebound effect.” Andrew would “behave like a wild man, out of control.” A doctor increased his dosage, only then it seemed that Andrew was like a “zombie,” his sense of humor reemerging only when the drug’s effects wore off. Next, Andrew needed to take clonidine in order to fall asleep at night. The drug treatment didn’t really seem to be helping, and so Ritalin gave way to other stimulants, including Adderall, Concerta, and dextroamphetamine. “It was always more drugs,” his mother says.
Medication Seen as Revealing Structural Flaws
One would think that the functional and structural deterioration that follows constant medication would cause both the patient and the doctor to reconsider the benefits of stabilisation. But this deterioration too can be interpreted in many different ways. Whitaker gives an example where the stabilised state is seen to be beneficial by revealing hitherto undiagnosed structural problems:
in 1982, Michael Strober and Gabrielle Carlson at the UCLA Neuropsychiatric Institute put a new twist into the juvenile bipolar story. Twelve of the sixty adolescents they had treated with antidepressants had turned “bipolar” over the course of three years, which—one might think—suggested that the drugs had caused the mania. Instead, Strober and Carlson reasoned that their study had shown that antidepressants could be used as a diagnostic tool. It wasn’t that antidepressants were causing some children to go manic, but rather the drugs were unmasking bipolar illness, as only children with the disease would suffer this reaction to an anti-depressant. “Our data imply that biologic differences between latent depressive subtypes are already present and detectable during the period of early adolescence, and that pharmacologic challenge can serve as one reliable aid in delimiting specific affective syndromes in juveniles,” they said.
Drug Withdrawal as Proof That It Works
The symptoms of drug withdrawal can also be interpreted to mean that the drug was necessary and that the patient is fundamentally ill. The reduction in withdrawal symptoms when the patient goes back on provides further “proof” that the drug works. Withdrawal symptoms can also be interpreted as proof that the patient needs to be treated for a longer period. Again, quoting from Whitaker:
Chouinard and Jones’s work also revealed that both psychiatrists and their patients would regularly suffer from a clinical delusion: They would see the return of psychotic symptoms upon drug withdrawal as proof that the antipsychotic was necessary and that it “worked.” The relapsed patient would then go back on the drug and often the psychosis would abate, which would be further proof that it worked. Both doctor and patient would experience this to be “true,” and yet, in fact, the reason that the psychosis abated with the return of the drug was that the brake on dopamine transmission was being reapplied, which countered the stuck dopamine accelerator. As Chouinard and Jones explained: “The need for continued neuroleptic treatment may itself be drug-induced.”
while they acknowledged that some alprazolam patients fared poorly when the drug was withdrawn, they reasoned that it had been used for too short a period and the withdrawal done too abruptly. “We recommend that patients with panic disorder be treated for a longer period, at least six months,” they said.
Similarly, macroeconomic crises can and frequently are interpreted as a need for better and more stabilisation. The initial positive impact of each intervention and the negative impact of reducing stimulus only reinforces this belief.
SCIENCE AND STABILISATION
A typical complaint against Whitaker’s argument is that his thesis is unproven. I would argue that within the confines of conventional “scientific” data analysis, his thesis and others directly opposed to it are essentially unprovable. To take an example from economics, is the current rush towards “safe” assets a sign that we need to produce more “safe” assets? Or is it a sign that our fragile economic system is addicted to the need for an ever-increasing supply of “safe” assets and what we need is a world in which no assets are safe and all market participants are fully aware of this fact?
In complex adaptive systems it can also be argued that the modern scientific method that relies on empirical testing of theoretical hypotheses against the data is itself fundamentally biased towards stabilisation and against resilience. The same story that I trace out below for the history of mental health can be traced out for economics and many other fields.
Desire to Become a ‘Real’ Science
Whitaker traces out how the theory attributing mental disorders to chemical imbalances was embraced as it enabled psychiatrists to become “real” doctors and captures the mood of the profession in the 80s:
Since the days of Sigmund Freud the practice of psychiatry has been more art than science. Surrounded by an aura of witchcraft, proceeding on impression and hunch, often ineffective, it was the bumbling and sometimes humorous stepchild of modern science. But for a decade and more, research psychiatrists have been working quietly in laboratories, dissecting the brains of mice and men and teasing out the chemical formulas that unlock the secrets of the mind. Now, in the 1980s, their work is paying off. They are rapidly identifying the interlocking molecules that produce human thought and emotion…. As a result, psychiatry today stands on the threshold of becoming an exact science, as precise and quantifiable as molecular genetics.
Search for the Magic Bullet despite Complexity of Problem
In the language of medicine, a ‘magic bullet’ is a drug that counters the root cause of the disease without adversely affecting any other part of the patient. The chemical-imbalance theory took a ‘magic bullet’ approach which reduced the complexity of our mental system to “a simple disease mechanism, one easy to grasp. In depression, the problem was that the serotonergic neurons released too little serotonin into the synaptic gap, and thus the serotonergic pathways in the brain were “underactive”. Antidepressants brought serotonin levels in the synaptic gap up to normal, and that allowed these pathways to transmit messages at a proper pace.”
Search for Scientific Method and Objective Criteria
Whitaker traces out the push towards making psychiatry an objective science with a defined method and its implications:
Congress had created the NIMH with the thought that it would transform psychiatry into a more modern, scientific discipline…..Psychiatrists and nurses would use “rating scales” to measure numerically the characteristic symptoms of the disease that was to be studied. Did a drug for schizophrenia reduce the patient’s “anxiety”? His or her “grandiosity”? “Hostility”? “Suspiciousness”? “Unusual thought content”? “Uncooperativeness”? The severity of all of those symptoms would be measured on a numerical scale and a total “symptom” score tabulated, and a drug would be deemed effective if it reduced the total score significantly more than a placebo did within a six-week period. At least in theory, psychiatry now had a way to conduct trials of psychiatric drugs that would produce an “objective” result. Yet the adoption of this assessment put psychiatry on a very particular path: The field would now see short-term reduction of symptoms as evidence of a drug’s efficacy. Much as a physician in internal medicine would prescribe an antibiotic for a bacterial infection, a psychiatrist would prescribe a pill that knocked down a “target symptom” of a “discrete disease.” The six-week “clinical trial” would prove that this was the right thing to do. However, this tool wouldn’t provide any insight into how patients were faring over the long term.
It cannot be emphasised enough that even increasing the period of the scientific trial is not enough to give us definitive answers. The argument that structural flaws are being uncovered or that withdrawal proves that the drug works cannot be definitively refuted. Moreover, at every point of time after medication is started, the short-term impact of staying on or increasing the level of medication is better than the alternative of going off the medication. The deeper issue here is also that in such a system, statistical analysis that tries to determine the efficacy of the intervention cannot deal with the fact that the nature of the intervention itself is to shift the distribution of outcomes into the tail and continue to do so as long as the level of medication keeps increasing.
The Control Agenda and High Modernism
The desire for stability and the control agenda is not simply a consequence of the growth of Olsonian special interests in the economy. The title of this post is inspired by Holling and Meffe’s classic paper on this topic in ecology. Their paper highlights that stabilisation is embedded within the command-and-control approach which itself is inherent to the high modernist way that James Scott has criticised.
Holling and Meffe also recognise that it is a simplistic application of “scientific” methods that underpins this command-and-control philosophy:
much of present ecological theory uses the equilibrium definition of resilience, even though that definition reinforces the pathology of equilibrium-centered command and control. That is because much of that theory draws predominantly from traditions of deductive mathematical theory (Pimm 1984) in which simplified, untouched ecological systems are imagined, or from traditions of engineering in which the motive is to design systems with a single operating objective (Waide & Webster 1976; De Angelis et. al. 1980; O’Neill et al. 1986), or from small-scale quadrant experiments in nature (Tilman & Downing 1994) in which long-term, large-scale successional or episodic transformations are not of concern. That makes the mathematics more tractable, it accommodates the engineer’s goal to develop optimal designs, and it provides the ecologist with a rationale for utilizing manageable, small sized, and short-term experiments, all reasonable goals. But these traditional concepts and techniques make the world appear more simple, tractable, and manageable than it really is. They carry an implicit assumption that there is global stability – that there is only one equilibrium steady-state, or, if other operating states exist, they should be avoided with safeguards and regulatory controls. They transfer the command-and-control myopia of exploitive development to similarly myopic demands for environmental regulations and prohibitions.
Those who emphasize ecosystem resilience, on the other hand, come from traditions of applied mathematics and applied resource ecology at the scale of ecosystems, such as the dynamics and management of freshwater systems (Fiering 1982) forests (Clark et al. 19759, fisheries (Walters 1986) semiarid grasslands (Walker et al. 1969), and interacting populations in nature (Dublin et al. 1990; Sinclair et al. 1990). Because these studies are rooted in inductive rather than deductive theory formation and in experience with the effects of large-scale management disturbances, the reality of flips from one stable state to another cannot be avoided (Helling 1986).
My aim in this last section is not to argue against the scientific method but simply to state that we have adopted too narrow a definition of what constitutes a scientific endeavour. Even this is not a coincidence. High modernism has its roots firmly planted in Enlightenment rationality and philosophical viewpoints that lie at the core of our idea of progress. In many uncertain domains, genuine progress and stabilisation that leads to fragility cannot be distinguished from each other. These are topics that I hope to explore in future posts.